Interaktion von humanen Makrophagen und Mycobacterium tuberculosis bei Hypoxie
Tuberculosis is one of the most common fatal bacterial diseases. The development of granulomas in the lung during the infection with Mycobacterium tuberculosis (M.tb) creates special conditions that are characterized by hypoxia. We hypothesized that hypoxic conditions modify the antimicrobial effector mechanisms of cells of the innate immunity, the macrophages. We established a hypoxia chamber in our S3 facility to exam the interaction of M.tb and macrophages. After securing the viability of macrophages and bacteria under hypoxia, we determined different parameters like phagocytosis, secretion of cytokines and chemokines and the intracellular growth of M.tb. in macrophages. We detected significant differences only at the reduced intracellular growth of 47% at hypoxic conditions compared with normoxia. Different antimicrobial peptides like cathelicidin and human beta-defensin-2 (hBD2) have been shown to suppress the growth of mycobacteria. Under hypoxia we detected a 3.6 time higher expression of hBD2 than under normoxic conditions but no differences in the expression of cathelicidin. Further experiments with the hypoxia chamber will help to understand the role of hypoxia and the modulation of the immune response and the antimicrobial effector mechanisms, like the expression of hBD2, against tuberculosis.
Erstellung / Fertigstellung
Normierte SchlagwörterHypoxie [GND]
Antimicrobial cationic peptides [MeSH]